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: 肝包虫蚴的建立与肝包虫病患者和小鼠模型中 CD4 T 细胞介导的免疫反应的控制有关。

: The establishment of the metacestode in the liver is associated with control of the CD4 T-cell-mediated immune response in patients with cystic echinococcosis and a mouse model.

机构信息

State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.

Basic Medical College, Xinjiang Medical University, Urumqi, China.

出版信息

Front Cell Infect Microbiol. 2022 Aug 15;12:983119. doi: 10.3389/fcimb.2022.983119. eCollection 2022.

DOI:10.3389/fcimb.2022.983119
PMID:36046744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9422084/
Abstract

The larval stage of the tapeworm () caused a chronic infection, known as cystic echinococcosis (CE), which is a worldwide public health problem. The human secondary CE is caused by the dissemination of protoscoleces (PSCs) when fertile cysts are accidentally ruptured, followed by development of PSCs into new metacestodes. The local immune mechanisms responsible for the establishment and established phases after infection with . are not clear. Here, we showed that T cells were involved in the formation of the immune environment in the liver in CE patients and ()infected mice, with CD4 T cells being the dominant immune cells; this process was closely associated with cyst viability and establishment. Local T2-type responses in the liver were permissive for early infection establishment by between 4 and 6 weeks in the experimental model. CD4 T-cell deficiency promoted PSC development into cysts in the liver in -infected mice. In addition, CD4 T-cell-mediated cellular immune responses and IL-10-producing CD8 T cells play a critical role in the establishment phase of secondary PSC infection. These data contribute to the understanding of local immune responses to CE and the design of new therapies by restoring effective immune responses and blocking evasion mechanisms during the establishment phase of infection.

摘要

绦虫的幼虫阶段()导致慢性感染,称为囊型包虫病(CE),这是一个全球性的公共卫生问题。人类继发性 CE 是由当成熟的包虫囊肿意外破裂时,原头蚴(PSCs)的传播引起的,随后原头蚴发育成新的包虫囊。导致感染后建立和确立阶段的局部免疫机制尚不清楚。在这里,我们表明 T 细胞参与了 CE 患者和感染()小鼠肝脏中免疫环境的形成,CD4 T 细胞是主要的免疫细胞;这一过程与囊肿的存活和建立密切相关。在实验模型中,在 4 至 6 周内,肝脏中的局部 T2 型反应允许在早期感染建立。CD4 T 细胞缺陷促进了感染小鼠肝脏中 PSC 向囊肿的发展。此外,CD4 T 细胞介导的细胞免疫反应和产生 IL-10 的 CD8 T 细胞在继发性 PSC 感染的建立阶段中发挥着关键作用。这些数据有助于了解对 CE 的局部免疫反应,并通过在感染的建立阶段恢复有效的免疫反应和阻断逃避机制来设计新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/346569e3eddf/fcimb-12-983119-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/a9847a630661/fcimb-12-983119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/2a326fef27de/fcimb-12-983119-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/754ba8074124/fcimb-12-983119-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/a85a5ae6d7e1/fcimb-12-983119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/6eed782300dd/fcimb-12-983119-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/346569e3eddf/fcimb-12-983119-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/a9847a630661/fcimb-12-983119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/2a326fef27de/fcimb-12-983119-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/754ba8074124/fcimb-12-983119-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/a85a5ae6d7e1/fcimb-12-983119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/6eed782300dd/fcimb-12-983119-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74c1/9422084/346569e3eddf/fcimb-12-983119-g006.jpg

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